Lipids 311increased HDL particle size (Baseline: 9.0 nm (SD 9.0) difference: 0.11 nm (0.1; 0.2), P<0.001).No changes were seen following AIT.No significant betweengroup differences were seen. Change in lipoprotein distributionConclusion: One year of LED+AIT increased the proportion of lipoprotein constituted by HDL, induced a shift in the HDL distribution and increased HDL particle size while no change was seen following AIT alone; however, no significant between group differences were seen.
OBJECTIVE—Diabetes, a major health problem worldwide, increases the risk of cardiovascular disease and its associated mortality. Evidence of the overall benefits of lipid modification in this area is needed. RESEARCH DESIGN AND METHODS—The Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID) trial showed that cholesterol-lowering treatment with pravastatin reduced mortality and coronary heart disease (CHD) events in 9,014 patients aged 31–75 years with CHD and total cholesterol 4.0–7.0 mmol/l. We measured the effects of pravastatin therapy, 40 mg/day over 6.0 years, on the risk of CHD death or nonfatal myocardial infarction and other cardiovascular outcomes in 1,077 LIPID patients with diabetes and 940 patients with impaired fasting glucose (IFG). RESULTS—In patients allocated to placebo, the risk of a major CHD event was 61% higher in patients with diabetes and 23% higher in the IFG group than in patients with normal fasting glucose, and the risk of any cardiovascular event was 37% higher in the diabetic group and 19% higher in the IFG group. Pravastatin therapy reduced the risk of a major CHD event overall from 15.9 to 12.3% (relative risk reduction [RRR] 24%, P < 0.001) and from 23.4 to 19.6% in the diabetic group (19%, P = 0.11); in the diabetic group, the reduction was not significantly different from the reductions in the other groups. Pravastatin reduced the risk of any cardiovascular event from 52.7 to 45.2% (21%, P < 0.008) in patients with diabetes and from 45.7 to 37.1% (26%, P = 0.003) in the IFG group. Pravastatin reduced the risk of stroke from 9.9 to 6.3% in the diabetic group (RRR 39%, CI 7–61%, P = 0.02) and from 5.4 to 3.4% in the IFG group (RRR 42%, CI −9 to 69%, P = 0.09). Pravastatin did not reduce the incidence of diabetes. Over 6 years, pravastatin therapy prevented one major CHD event (CHD death or nonfatal myocardial infarction) in 23 patients with IFG and 18 patients with diabetes. A meta-analysis of other major trials confirmed the high absolute risks of diabetes and IFG and the absolute benefits of statin therapy in these patients. CONCLUSIONS—Cholesterol-lowering treatment with pravastatin therapy prevents cardiovascular events, including stroke, in patients with diabetes or IFG and established CHD.
Summary: The diagnostic and potential therapeutic value of rapid right atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction, was examined. The effect of right atrial pacing at incremental rates beginning 10 bpm above the rate of the tachycardia was studied in five patients with ventricular tachycardia, and in four patients with supraventricular tachycardia with rate‐related bundle branch block aberration, the mechanism of tachycardia having been demonstrated at electrophysiology study. Atrial pacing resulted in persistent (four) or occasional (one) normalisation of the QRS complexes to that seen in sinus rhythm in those five patients with ventricular tachycardia. The intraventricular conduction pattern persisted with atrial pacing in those patients with supra‐ventricular tachycardia and aberrant intraventricular conduction. This confirms that atrial pacing is a useful and simple diagnostic test in wide QRS tachycardia, which does not require sophisticated electrophysiological facilities. In three of the patients with ventricular tachycardia, atrial pacing terminated the arrhythmia, suggesting potential therapeutic use of rapid atrial pacing in such patients.
To examine the effectiveness of different strategies for recruiting participants for a large Australian randomised controlled trial (RCT), the Australian Study for the Prevention through Immunisation of Cardiovascular Events (AUSPICE).Men and women aged 55-60 years with at least two cardiovascular risk factors (hypertension, hypercholesterolaemia, overweight/obesity) were recruited for a multicentre placebo-controlled RCT assessing the effectiveness of 23-valent pneumococcal polysaccharide vaccine (23vPPV) for preventing cardiovascular events.Invitations were mailed by the Australian Department of Human Services to people in the Medicare database aged 55-60 years; reminders were sent 2 weeks later. Invitees could respond in hard copy or electronically. Direct recruitment was supplemented by asking invitees to extend the invitation to friends and family (snowball sampling) and by Facebook advertising.Proportions of invitees completing screening questionnaire and recruited for participation in the RCT.21 526 of 154 992 invited people (14%) responded by completing the screening questionnaire, of whom 4725 people were eligible and recruited for the study. Despite the minimal study burden (one questionnaire, one clinic visit), the overall participation rate was 3%, or an estimated 10% of eligible persons. Only 16% of eventual participants had responded within 2 weeks of the initial invitation letter (early responders); early and late responders did not differ in their demographic or medical characteristics. Socio-economic disadvantage did not markedly influence response rates. Facebook advertising and snowball sampling did not increase recruitment.Trial participation rates are low, and multiple concurrent methods are needed to maximise recruitment. Social media strategies may not be successful in older age groups.Australian New Zealand Clinical Trials Registry, ACTRN12615000536561.
High office blood pressure variability (OBPV) in midlife increases the risk of cardiovascular disease (CVD), but the impact of OBPV in older adults without previous CVD is unknown. We conducted a post hoc analysis of ASPREE trial (Aspirin in Reducing Events in the Elderly) participants aged 70-years and older (65 for US minorities) without history of CVD events at baseline, to examine risk of incident CVD associated with long-term, visit-to-visit OBPV. CVD was a prespecified, adjudicated secondary end point in ASPREE. We estimated OBPV using within-individual SD of mean systolic BP from baseline and first 2 annual visits. Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% CI for associations with CVD events. In 16 475 participants who survived to year 2 without events, those in the highest tertile of OBPV had increased risk of CVD events after adjustment for multiple covariates, when compared with participants in the lowest tertile (HR, 1.36 [95% CI, 1.08-1.70]; P=0.01). Similar increased risk was observed for ischemic stroke (HR, 1.56 [95% CI, 1.04-2.33]; P=0.03), heart failure hospitalization, or death (HR, 1.73 [95% CI, 1.07-2.79]; P=0.02), and all-cause mortality (HR, 1.27 [95% CI, 1.04-1.54]; P=0.02). Findings were consistent when stratifying participants by use of antihypertensive drugs, while sensitivity analyses suggested the increased risk was especially for individuals whose BP was uncontrolled during the OBPV estimation period. Our findings support increased OBPV as a risk factor for CVD events in healthy older adults with, or without hypertension, who have not had such events previously. Registration- URL: https://www.clinicaltrials.gov; Unique identifiers: NCT01038583; URL: https://www.isrctn.com; Unique identifiers: ISRCTN83772183.
Cardiovascular mortality is higher in New Zealand compared to Australia, but reasons for this difference are uncertain. This study describes differences in cardiovascular risk factors and cardiovascular mortality in Australians and New Zealanders with stable coronary artery disease stratified by socioeconomic status.Socioeconomic status was estimated from the residential area of 5949 Australians and 2784 New Zealanders with a history of myocardial infarction or unstable angina who participated in the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study. Socioeconomic and international differences in cardiovascular risk factors, medical treatments, and cardiovascular mortality during a median follow-up period of 7.8 years were evaluated.Cardiovascular mortality increased as the median residential-area income decreased in both Australia (hazard ratio [HR]/income tertile 1.20, 95% confidence interval [CI] 1.08-1.32) and New Zealand (HR 1.16, 95%CI 1.02-1.31), but was higher in New Zealand across all socioeconomic groups (HR 1.42, 95%CI 1.25-1.61). Obesity, smoking, and a high white blood cell count at baseline were associated with higher cardiovascular mortality and were more common in lower-income areas in both countries. The total:HDL cholesterol ratio was higher in New Zealand, but similar across all socioeconomic groups. In both countries there were socioeconomic gradients in open-label usage of cholesterol-lowering medication, percutaneous coronary intervention, and coronary artery bypass surgery. However, Australians in all socioeconomic groups were more likely than New Zealanders to receive these treatments.Although there is an important socioeconomic gradient in cardiovascular mortality in both Australia and New Zealand, cardiovascular mortality is higher in New Zealanders than Australians with stable coronary disease from all socioeconomic groups.
Lower socioeconomic status (SES) is associated with a higher prevalence of major risk factors for cardiovascular disease (CVD). However, few longitudinal studies have examined the association between SES and CVD risk factors over time. We aimed to determine whether SES, using education as a proxy, is associated with the onset of CVD risk factors over 5 years in an Australian adult cohort study. Participants in the Australian Diabetes, Obesity and Lifestyle study (AusDiab) study aged 25 years and over who attended both baseline and 5-year follow-up examinations (n=5 967) were categorised according to educational attainment. Cardiovascular risk factor data at both time points were ascertained through questionnaire and physical measurement. Women with lower education had a greater risk of progressing from normal weight to overweight or obesity than those with higher education (age-adjusted OR 1.57, 95% CI 1.06-2.31). Both men and women with lower education were more likely to develop diabetes (age-adjusted OR from higher education 1.75, 95% CI 1.14-2.71 and 3.01, 95% CI 1.26-7.20, respectively). A lower level of education was associated with a greater number of risk factors accumulated over time in women (OR of progressing from having two or less risk factors at baseline to three or more at follow up, 2.04, 95% 1.32-3.14). In this Australian population-based study, lower educational attainment was associated with an increased risk of developing both individual and total CVD risk factors over a 5-year period. These findings suggest that SES inequalities in CVD will persist into the future.
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